Air-breathing changes the pattern for temperature-induced pH regulation in a bimodal breathing teleost.

Abstract

It is well established that ectothermic vertebrates regulate a lower arterial pH when temperature increases. Typically, water-breathers reduce arterial pH by altering plasma [HCO3-], whilst air-breathers rely on ventilatory adjustments to modulate arterial PCO2. However, no studies have investigated whether the shift from water- to air-breathing within a species changes the mechanisms for temperature-induced pH regulation. Here, we used the striped catfish Pangasianodon hypophthalmus to examine how pH regulation is affected by water- versus air-breathing, since P. hypophthalmus can accommodate all gas exchange by its well-developed gills in normoxic water, but achieves the same metabolic rate with aerial oxygen uptake using its the swim-bladder when exposed to aquatic hypoxia. We, therefore, measured arterial acid-base status in P. hypophthalmus as temperature changed between 20 and 35°C in either normoxic or severely hypoxic water. In normoxic water, where P. hypophthalmus relied entirely on branchial gas exchange, P. hypophthalmus exhibited the typical teleost reduction in plasma [HCO3-] and arterial pH when temperature rose. However, when forced to increase air-breathing in hypoxic water, arterial PCO2 fell due to a branchial hyperventilation, but it increased with temperature most likely due to passive CO2 retention. We propose that the rise in arterial PCO2 reflects a passive consequence of the progressive transition to air breathing at higher temperatures, and that this response fortuitously matches the new regulated pHa, relieving the requirement for branchial ion exchange.